PHOSPHINE
International Programme on Chemical Safety
Poisons Information Monograph 865
Chemical
1. NAME1.1 SubstancePhosphine1.2 GroupPhosphorous hydride1.3 SynonymsHydrogen phosphide; trihydrogen phosphide;
phosphorus trihydrides; phosphoretted hydrogen; 2phospane;
celphos; delicia; detia; gas-ex-B; celphos1.4 Identification numbers1.4.1 CAS number
7803-51-21.4.2 Other numbers
DOT UN 2199 (DOT = Dept. of Transport)1.5 Main brand names/Trade namesAl Pare Alutal; Celphide; Celphine; Celphos; Delicia Gas
toxin; Detia Gas Ex-B/P/T; L-Fume; Phosphine; Phostex;
Phostoxin; Quickfos; Zedesa1.6 Main manufacturers/main importersTo be completed by each poison control centre.2. SUMMARY2.1 Main risks and target organsPhosphine is a colourless gas which is odourless when
pure, but the technical product has a foul odour, described
as "fishy" or "garlicky", because of the presence of
substituted phosphine and diphosphine (P2H4).
Other impurities may be methane, arsine, hydrogen and
nitrogen. For fumigation, it is produced at the site of
hydrolysis of a metal phosphide (AlP, Zn3P2, Mg3P2)
and supplied in cylinders either as pure phosphine or diluted
with nitrogen.
Phosphine is flammable and explosive in air and can
autoignite at ambient temperatures. It is slightly soluble
in water and soluble in most organic solvents. Metal
phosphides are usually powders of various colours, which
hydrolyse to yield phosphine and metal salts.
Inhalation of phosphine may cause severe pulmonary irritation
leading to acute pulmonary oedema, cardiovascular
dysfunction, CNS excitation, coma and death.
Gastrointestinal disorders, renal damage and leukopenia may
also occur.
Exposure to 1400 mg/m3 (1000 ppm) for 30 minutes may be
fatal.
Ingestion of phosphides, particularly aluminum and zinc
phosphides, may induce severe gastrointestinal irritation
leading to haemorrhage, cardiovascular collapse, acute
neuropsychiatric disorders, respiratory and renal failure
within a few hours. Hepatic damage may develop later.2.2 Summary of clinical effectsInitial clinical manifestations of mild phosphine
inhalation mimic an upper respiratory tract infection. Other
symptoms may include nausea, vomiting, diarrhoea, headache,
fatigue and dizziness. In severe exposure, lung irritation
with persistent coughing, ataxia, paraesthesia, tremor,
diplopia and jaundice may also occur. Very severe cases may
progress to acute pulmonary oedema, cardiac dysrhythmias,
convulsions, cyanosis and coma. Oliguria, proteinuria and
finally anuria may be induced.
Deliberate ingestion of phosphides, especially AID
(Phostoxin), causes nausea, vomiting, and sometimes
diarrhoea, retrosternal and abdominal pain, tightness in the
chest and coughing, headache and dizziness. In severe cases,
gastrointestinal haemorrhage, tachycardia, hypotension,
shock, cardiac arrhythmias, hypothermia, metabolic acidosis,
cyanosis, pulmonary oedema, convulsions, hyperthermia and
coma may occur. Clinical features of renal insufficiency and
hepatic damage including oliguria, and jaundice may develop
later, if the patient does not die.
Death, which may be sudden, usually occurs within four days
but may be delayed for one to two weeks. Postmortem
examinations have revealed focal myocardial infiltration and
necrosis, pulmonary oedema and widespread small vessel
injury.
Chronic poisoning from inhalation or ingestion of
phosphine/phosphides may cause toothache, swelling of the
jaw, necrosis of mandible, weakness, weight loss, anaemia,
and spontaneous fractures.2.3 DiagnosisMajor accidental release of stored phosphine presents
serious toxic and explosion/fire hazards for man and even
animals. The diagnosis of phosphine poisoning is easy, but
the clinical manifestations of phosphine and the phosphides
may be similar to those of other toxic chemicals such as
arsenic sulphide and calcium oxide. A silver nitrate-
impregnated paper test can be used for the breath and gastric
fluid of the patients exposed to phosphine/phosphide: silver
nitrate and phosphine/phosphides react to form silver
phosphide which confirms the diagnosis. Other laboratory
investigations such as cell blood counts, haemoglobin,
haematocrit, arterial blood gas analyses, renal and liver
function tests and cardiopulmonary monitoring and
investigations (ECG and chest X-ray) are essential for the
assessment of organ effects and the management of
phosphine/phosphide poisoning.2.4 First aid measures and management principlesRemove the patient from exposure site, and keep at rest.
If the patient is unconscious and breathing stops,
immediately ventilate artificially and if the heart stops,
begin cardiopulmonary resuscitation. In case of ingestion,
after consideration of tracheal intubation, perform gastric
aspiration and lavage with cold water and preferably sodium
bicarbonate solution (2%). Do not give milk, fats or saline
emetics. Administration of repeated doses of activated
charcoal through the gastric tube may be useful. Monitor and
support vital functions, particularly cardiopulmonary, G.I.,
renal and hepatic functions.
Treat shock conventionally and correct acidosis based on
blood gas analyses.
No antidote is available for phosphine/phosphide poisoning.
Early recognition and management of the poisoning is
essential.3. PHYSICO-CHEMICAL PROPERTIES3.1 Origin of substancePhosphine is extremely rare in nature. It occurs
transiently in marsh gas and other sites of anaerobic
degradation of phosphorus-containing matter.
Although phosphorus could be expected to occur naturally as a
phosphide, the only phosphide in the earth's crust is found
in iron meteorites as the mineral schreibersite (Fe,Ni)3P,
in which cobalt and copper may also be found (WHO, 1988).
Atmospheric phosphine results from emission and effluents
from industrial processes and from the use of phosphides as
rodenticides and fumigants.
Unexpected focal release of phosphine may occur due to the
action of water on phosphides present as impurities in some
industrial materials. Although some phosphine is supplied in
cylinders, it is often produced as and when required, by
hydrolysis of a metal phosphide. Phosphine is also produced
as a by-product or evolved incidentally in various industrial
processes (WHO, 1988; Casarett, 1991).3.2 Chemical structurePhosphine is trihydrogen phosphide
Molecular formula: PH3
Molecular weight: 34
Metal phosphides that are commonly used as rodenticide and
fumigants are:
zinc phosphide (Zn3P2, CAS No. 1314-84-7, molecular
weight = 258.1)
aluminum phosphide (AlP, CAS No. 20859-73-8, molecular weight
= 57.96)
magnesium phosphide (Mg3P2, CAS No. 12057-74-8, molecular
weight = 134.87)
(Deichman & Gerarde, 1964; WHO, 1988).3.3 Physical properties3.3.1 Colour
Colourless3.3.2 State/form
Gas3.3.3 Description
Pure phosphine is a colourless gas at ambient
temperature and pressure.
Melting point: -133.5°C
Boiling point -87.4°C
Phosphine is odourless when pure, at least up to a
concentration of 282 mg/m3 (200 ppm), which is
highly toxic level. The odour of technical phosphine
depends on the presence of odoriferous impurities and
their concentrations and odour threshold is usually in
the range 0.14 to 7 mg/m3.
Pure phosphine has an autoignition temperature of
38°C, but because of the presence of other phosphorus
hydrides, particularly diphosphine (P2H4), as
impurities, the technical product often ignites
spontaneously at room temperature.
Phosphine has intense ultraviolet absorption in the
185 to 250 nm (1850 to 2000 A) region.3.4 Hazardous characteristicsPhosphine forms explosive mixtures with air at
concentrations greater than 1.8%. The relative molecular
mass of phosphine is 34. It dissolves in water to form a
neutral solution, but its water solubility is very low (0.25
at room temperature). Phosphine dissolves more easily in
organic solvents, particularly in trifluoroacetic acid and
carbon disulphide (Beliles, 1981).
In air, the upper and lower explosion limits depend on the
temperature, pressure, and proportion of phosphine, oxygen,
inert gases and water vapour present, and also on the level
of ultraviolet irradiation. In aqueous solutions, oxidation
of phosphine results in the production of hypophosphorous
acid.
The technical grade of phosphine contain impurities of higher
phosphines (diphosphine) and substituted phosphines, which
are responsible for the characteristic foul odour of
phosphine which is often described as "fishy" or
"garlicky".
Depending on the method of manufacturer, other impurities may
include methane, arsine, hydrogen and nitrogen (Polson et
al., 1983).
An important reaction of phosphine is with metal, especially
with copper and copper-containing alloys, which causes severe
corrosion. The reaction is enhanced in the presence of
ammonia or moisture and salt. Eighteen carat gold jewellery
reacts at one-eighth of the rate of copper (WHO, 1988).
Phosphine and the metal phosphides have only been detected in
the general environment in relation to the recent use of
metal phosphides in pest control and in relation to a number
of industrial activities.
The metal phosphides are solid with grey colour and melting
points of more than 750°C. They hydrolyse very quickly and
produce phosphine which is more toxic than the metal
phosphide.
The volumes released in industrial operations are much
smaller and are therefore of less significance in relation to
atmospheric pollution.
Residues in fumigated foods are 0.01 mg/m3 (0.01 ppm) or
less and are negligible. Higher residue levels may be found
with storage at low temperature. About 10% of the residues
are water soluble and appear to be hypophosphite and
pyrophosphate. The remainder may have included insoluble
aluminium salts (WHO 1988).
Residue levels of phosphine in fumigated foods are generally
regulated at 0.1 mg/kg (0.1 ppm) or sometimes 0.01 mg (0.01
ppm). However, among populations whose diet in mainly derived
from stored products, the daily intake would be unlikely to
exceed 0.1 mg/day, even if the phosphine and phosphides
survived cooking.4. USES/HIGH RISK CIRCUMSTANCES OF POISONING4.1 Uses4.1.1 Uses
FumigantsPesticide for use on vertebrate animals4.1.2 Description
Phosphine is mainly used as a fumigant in pest
control. Zinc phosphide is used as a rodenticide
because of its reaction with stomach acid in the
rodent to release phosphine. For fumigation, the acid
has to be supplied. Since they hydrolyse in neutral
moist conditions, aluminum and magnesium phosphides
are preferred as fumigants. Aluminum phosphide has
also been used as a rodenticide; magnesium phosphide
may be used as a pesticide.
Zinc phosphide is available in bulk, typically to a
specification of at least 80% Zn3P2, and as paste
containing 5% or 2.5% for use as a rodenticide by
mixing in bait. Aluminum and magnesium phosphides are
available in a number of commercial formulations.
Aluminum phosphide formulations usually contain
approximately 75% active ingredient and magnesium
phosphide products contain 43% active ingredient (WHO,
1988).4.2 High risk circumstances of poisoning.No subgroups of the general population have been
identified to be at special risk from phosphine and the
phosphides except children, who might find and eat bait
containing phosphides. Zinc phosphide pastes and tablets of
zinc, aluminum and magnesium phosphides which are available
without restriction in some countries may be used in suicide
attempts. Many reports of high mortality (&gt 50%) due to
metal phosphide poisonings in India have recently been
published.4.3 Occupationally exposed populations.Occupational exposure can be divided into 4 general
categories: (a) workers producing phosphine and phosphides;
(b) workers in operations that can release phosphine, e.g.,
welding, metallurgy, semi-conductors (c) fumigators and
pest-control operators; and (d) transport workers. e.g.
drivers, seamen. Exposure patterns and the potential for
control of exposure differ from case to case.
Exposure to phosphine and phosphorus oxides, which occurs
during the manufacture of metal phosphides, varies according
to the method of manufacture. High levels of exposure may
occur in the direct methods involving the reaction of red
phosphorus with powdered metal, in which the air phosphine
concentrations of 0.4 to 1.6 mg/m3 (0.3 to 1.13 ppm) may
occur. Concentration of &gt 2 mg/m3 require the use of
personal respiratory protection.
In recorded cases, atmospheric levels to which operatives
were exposed while adding zinc/aluminum phosphides to wheat
were undetectable. Levels encountered when stores were
re-entered for loading or turning were much higher, ranging
from 18 to 35 mg/m3 (13 to 25 ppm).
Exposure to phosphine has also been described in the
operation of acetylene generators and in the production of
phosphorus. A badly ventilated cargo of ferrosilicon,
particularly in barges, can release phosphine accidentally by
the reaction of water with calcium phosphide, one of the
impurities present.
Many metals contain phosphorus in small amounts, and
phosphine can be generated in a variety of metallurgical
processes.
Although phosphine is used extensively in semi-conductor
manufacture, there are no published figures for occupational
exposure in this industry. There are also no published data
relating to exposure to phosphine in the synthesis of
organophosphine or phosphonium derivatives. The occupational
exposure limit for phosphine in various countries differ from
0.1 mg/m3 to 0.5 mg/m3 in long term and up to 1.5 mg/m3
(1.1 ppm) in short term exposure (WHO, 1988; Deichmann &
Gerarde, 1969).5. ROUTES OF EXPOSURE5.1 OralDeliberate oral ingestion of the metal phosphides,
particularly AlP (Phostoxin), is not rare in some parts of
the world. Accidental oral ingestion of the metal
phosphides, particularly zinc phosphide, have also been
reported.5.2 InhalationInhalation is the commonest route of phosphine
poisoning.5.3 DermalThe skin is not a common route of absorption of
phosphine and phosphides. However, dermal absorption of zinc
phosphide in rabbits was reported by US National Pest Control
Association (WHO, 1988).5.4 EyeNo data available.5.5 ParenteralStephenson (1967) mentioned the possibility of zinc
phosphide injection.5.6 OthersNo data available.6. KINETICS6.1 Absorption by route of exposureInhaled phosphine is generally considered to be rapidly
absorbed through the lungs. After inhalation, aluminum and
magnesium phosphides deposited on the moist surfaces of the
respiratory tract would release phosphine, but zinc
phosphide, which hydrolyses significantly only under acid
conditions, would be stable for some time. However, the
transfer of a proportion of inhaled zinc phosphide to the
intestinal tract by particulate clearance mechanisms in the
lung would permit hydrolysis to phosphine by gastric acid, as
well as absorption of the zinc phosphide. The lung also
absorbs particles and it is known that zinc phosphide is
absorbed intact from the gut. Inhaled zinc phosphide dust
might be absorbed directly via the respiratory tract and then
hydrolysed in the tissues.
In the rat, ingestion of zinc phosphide results in detectable
amounts of acid-hydrolysable phosphide in the liver. Human
ingestion of tablets containing aluminum phosphide yielded
evidence of acid-hydrolysable phosphide in blood and liver.
These results indicate that metal phosphides can be absorbed
directly. In the rat, recovery of phosphide from the
following administration of zinc phosphide in corn oil was 4
times higher than when administered in water, suggesting that
absorption of unhydrolysed material is greater.
In general, dermal absorption of phosphine and phosphides is
insignificant.6.2 Distribution by route of exposureInhaled phosphine produces neurological and hepatic
symptoms suggesting that it reaches the nervous system and
liver. Ingested phosphides have been shown to reach the
blood and liver in rats and human beings. On the other hand,
muscle tissue of animals poisoned with supralethal doses of
zinc phosphide does not contain detectable levels of
phosphine or phosphide and does not produce toxic effects
when fed to test animals. The presence of acid-hydrolyzable
phosphide in the kidney and liver of a fatal case of zinc
phosphide has been reported (WHO, 1988).6.3 Biological half-life by route of exposureThe biological half-life of phosphine and phosphides in
man has not been reported and may be difficult to estimate.
Experimentally, the amount of acid-hydrolyzable phosphide
found in the liver of a rat fed phosphide for 15 days is
nearly twice that of a rat fed for 7 days. However, this
limited study cannot be considered to provide evidence of a
long biological half-life and/or the accumulation of metal
phosphides (WHO, 1988).6.4 MetabolismMetal phosphides are hydrolysed to phosphine. In the
rat, phosphine that is not excreted in the expired air is
oxidized and appears in the urine, chiefly as hypophosphite
and phosphite. The fact that (a) phosphine is incompletely
oxidized; and (b) the proportion of an administered dose that
is eliminated as expired phosphine increases with the dose,
suggests that the oxidative pathway is slow (WHO, 1988).
Oxyhaemoglobin is denatured and a variety of enzymes are
inhibited by reaction with phosphine (WHO, 1988).6.5 Elimination and excretionZinc phosphide suspended in corn oil was given to rats
by gavage and phosphine concentrations were measured in a
metabolic chamber over the following 12 hours. After doses
of 0.5, 1, 2, 3 and 4 mg, the proportions of the administered
doses as phosphine were 1.5%, 1.7%, 3.2%, 15.6% and 23.5%,
respectively, but some or much of this could have been
derived from faeces or intestinal gas rather than by
desorption and exhalation. Hypophosphite is the principal
urinary excretion product (WHO, 1988).7. TOXICOLOGY7.1 Mode of actionPhosphine reduces the respiration of wheat partly by
damaging the microflora present. The activity of glutamate
decarboxylase is reduced when the moisture content is 18% or
more. Alcohol dehydrogenase activity is reduced to zero
within 7 days as a result of phosphine treatment of the grain
at a moisture content of more than 24%. Catalase activity in
wheat is reduced by about 20% after 2 weeks exposure to
phosphine fumigations. Phosphine markedly inhibits
respiration and the growth of microorganisms in wheat with a
moisture content up to 29%. The amount of adenosine
triphosphate (ATP) is reduced by phosphine fumigation, but
adenosine diphosphate (ADP) is not, indicating that the
respiratory activity in treated grain is markedly reduced
(WHO, 1988).
Studies on isolated rat liver showed that mitochondrial
oxygen uptake is inhibited by phosphine due to its reaction
with cytochrome C and cytochrome C oxidase. Phosphine
inhibits insect catalase, though this appears to be an
indirect effect and might be a consequence not a cause of
toxicity.
There have not been any systemic studies on the mechanism of
phosphine toxicity in man. Various effects on intermediary
metabolism have been described. Dose-related increases in
blood and urinary porphyrin concentrations due to zinc
phosphide have been reported. In a study on rabbits, changes
in serum glutamic-pyruvic and glutamic oxalacetic
transaminase, leucine aminopeptidase, aldolase, alkaline
phosphatase and albumin in the first 24 hours of zinc
phosphide poisoning have been observed. Dysfunction of
hepatic fat metabolism was also reported. Loss of cell
viability and cell membrane integrity accounts for the raised
hepatic enzymes and the bronchiolitic effect. There is no
adequate explanation for the fact that phosphine does not
cause the haemolysis that is characteristic of arsine.
Although the exact mechanism of action of phosphine in man is
not known, non-competitive inhibition of mitochondrial
cytochrome oxidase in mouse liver, housefly and granary
weevil is mentioned by some authors (Singh et al., 1985;
Chopra et al., 1986; Khosta et al., 1988).7.2 Toxicity7.2.1 Human data
7.2.1.1 Adults
Phosphine and the metal phosphides
are highly toxic to human beings and
animals.
The odour of phosphine depends on the
impurities it contains. When pure it has no
odour, even at a concentration of 28 mg/m3.
Phosphine prepared conventionally without
purification, has a fishy or garlic-like
odour due to its impurities. These may be
absorbed by stored products during fumigation
with a resultant loss of odour, even though
phosphine remains at toxic concentrations.
Phosphine is in class D of the safety
classification, because 20 to 50% of
attentive persons can detect the threshold
limit value (TLV) of 0.42mg/m3 by smell.
However, the smell of phosphine cannot be
relied on as a warning of toxic
concentrations.
Zinc phosphide baits and formulated aluminium
phosphide pellets are widely used.
Occasional accidental or more usually
suicidal exposure to the metal phosphides may
be encountered. Ingestion, the only highly
toxic route, has almost always been with
suicidal intent and the symptoms are always
acute.
There is negligible exposure of the general
population to phosphine. Many cases of acute
phosphine poisoning due to occupational
exposure have been reported in the literature
(WHO, 1988).
In one incident, 12 inhabitants of an
apartment house developed nausea and one died
when phosphine was emitted from an adjacent
warehouse containing bags of aluminum
phosphide which became damp. Some passengers
on ships and barges carrying cargoes of
ferrosilicon of grain under fumigation have
also been poisoned by phosphine, with
symptoms similar to those of acute
occupational poisoning. In a further
incident, 2 adults and one child died when a
granary sharing a party wall with their house
was fumigated. It was estimated that
phosphine concentration in the bedroom
reached 1.2 mg/m3. Symptoms were initially
non-specific and insidious and illustrate the
risk of sustained exposures to relatively low
concentrations. At autopsy, there was
congestion of all organs; pulmonary oedema
and focal emphysema were found in the lungs
and there was vacuolation in the liver (WHO,
1988).
Many cases of acute deliberate zinc phosphide
poisoning by ingestion have been reported in
the literature. Stephenson (1967) reviewed
20 patients with zinc phosphide poisoning by
ingestion in which the approximate doses were
recorded. Of these, 10 patients died after
ingestion of 4.5 to 180 g; 6 cases had
ingested 20 g or more. In the 10 non-fatal
cases, the doses ranged from 0.5 to 50 g and
7 ingested less than 20 g. The main clinical
manifestations were metabolic acidosis,
methaemoglobinaemia, hypocalcaemic tetani,
reduced blood coagulation, pulmonary oedema;
and gastrointestinal, neuropsychiatric and
cardiovascular disorders. Postmortem
findings included blood in all the serous
cavities, pulmonary congestion and oedema,
haemorrhagic changes in the intestinal
epithelium, centrilobular congestion and
necrosis and yellow discolouration of the
liver, and patchy necrosis of the proximal
convoluted - tubules of the kidneys.
An unsuccessful suicidal attempt by a 25
year-old man who ingested 6 tablets of AID
(Phostoxin) in water was reported. Immediate
symptoms were severe retrosternal pain, a
generalized burning sensation and vomiting.
There was circulatory collapse necessitating
resuscitation and subsequently cerebral,
renal and hepatic dysfunction appeared.
Harger and Spobyar (1958) reviewed 54 cases
of acute phosphine poisoning with 26 deaths
since 1900. In 6 of 11 reports, cargoes of
ferrosilicon were cited as the source of
phosphine and in these cases, the victims
were passengers or crew members of the ships
or barges concerned. Other cases involved
the exposure of welders to calcium carbide
and raw acetylene and of submariners to
sodium phosphide. The most common autopsy
finding was congestion of the lungs with
marked oedema.
Metal workers at a large shipyard in Norway,
drilling deep holes in spheroidal graphite
iron, became ill during work. The symptoms
were mostly nausea, dizziness, chest
tightness, dyspepsia and disturbances of
smell and taste. Measurement of phosphine
concentration in the worker's breathing zone
(with Drager tubes) showed a phosphine
concentration of about 1.4 mg/m3 (1 ppm).
After installing local exhaust ventilation on
the drilling machines, there were no longer
any measurable amounts of phosphine, and
there were no complaints from the workers.
When the local exhaust ventilation was
removed for technical reasons 5 years later
illness among the workers recurred.
Measurement of phosphine levels just above
the machines, showed concentration up to 56
to 70 mg/m3 (40 to 50 ppm). When the local
exhaust ventilation was re-installed, the
phosphine concentrations dropped to
unmeasurable amounts, and no further cases
were reported. (WHO 1988).7.2.1.2 Children
Two children and 29 of 31 crew
members aboard a grain freighter became
acutely ill after inhaling the toxic fumigant
phosphine; one child died. Predominant
symptoms were headache, fatigue, nausea,
vomiting, cough and shortness of breath.
Abnormal physical findings included jaundice,
paraesthesia, ataxia, intention tremor and
diplopia. Focal myocardial infiltration with
necrosis, pulmonary oedema and widespread
small vessel injury were found postmortem.
The surviving child showed ECG and
echocardiographic evidence of myocardial
injury and transient elevation of MB fraction
of serum creatinine phosphokinase. Phosphine
gas was found to have escaped from the holds
through a cable housing located near the
midship ventilation intake and around hatch
covers on the forward deck (Wilson et al.,
1980).
Occasional reports on accidental phosphine
poisoning in children have been
published.
Reports of deaths of children and adults in
chemical accidents involving phosphine have
been published (Wilson et al., 1980).
Acute phosphine poisoning following ingestion
of aluminum phosphide has been reported in
young children and adults. Eight patients
aged 14 to 25 years with acute aluminum
phosphide poisoning reported by Misra et al.
(1988). The clinical picture consisted of
acute gastritis, altered sensorium and
peripheral vascular failure, cardiac
arrhythmias, jaundice and renal failure. Six
patients died, the mean hospital stay was 19
(range 4 to 72) hours. These patients had
taken 2 or more AlP tablets, whereas the two
patients survived had taken one tablet or
less.
Postmortem examination revealed pulmonary
oedema, gastrointestinal mucosal congestion,
and petechial haemorrhages on the surface of
liver and brain.7.2.2 Relevant animal data
Animal experiments have revealed that rabbits
exposed to 70 mg phosphine/m3 (50 ppm) for 10
minutes do not develop any symptoms but exposure to
140 mg/m3 (500 ppm) is fatal in 2.5 to 3 hour, and
700 mg/m3 (500 ppm) is fatal 25 to 30 minutes. Rats
survive exposure to 80 and 800 mg/m3 for 4 and 1
hour, respectively. All animals exhibited signs of
respiratory irritation and died of pulmonary oedema.
Pathological examination of the lungs revealed
bronchiolitis and atelectasis; there was no evidence
of haemolysis but all organs were hyperaemic. The
liver showed fatty infiltration and there was cloudy
swelling of kidney tubular cells. Neurohistological
studies in rats revealed widening of the perivascular
spaces, vacuolization of the nuclei of ganglion cells,
a reduction in the Purkinje cells and a glial
reaction. In one study a 4-hour LC50 for phosphine
inhalation in male rats was estimated as 15 mg/m3
(11 ppm), but in another study on female rats it was
reported as 55 mg/m3. The LC95 was 420 (260 to
670) mg/h/m3. The US National Pest Control
Association submitted a value of 19.6 mg/L for an
inhalation LC50 of 10% zinc phosphide powder in
rats.
In an oral study on 35 rats of both sexes administered
doses of 20, 40, 50 and 80 mg/kg LD50 for zinc
phosphide was 40.5 to 2.9 mg/kg body weight. The
LD50 for kit fox was reported as 93 mg zinc
phosphide/kg body weight. A dose of 100 mg/kg
bodyweight of zinc phosphide was fatal for dogs after
starving but not after feeding.
An acute dermal LD50 of 2000 to 5000 mg/kg body
weight for zinc phosphide (94% Zn3P2) in rabbits
is reported by the US National Pest Control
Association (WHO, 1988).
Inhalation exposure to phosphine at 28 mg/m3 (20
ppm) for 4 hours a day was fatal for rabbits and
guinea pigs. Pretreatment with sub-lethal
concentrations of phosphine reduced resistance to
near-lethal concentrations. At low concentrations (up
to 14 mg/m3), animals displayed no signs until about
0.5 hour before death when they exhibited diminished
reactivity, became stuporous with shallow respiration
and died in coma and occasionally with signs of
pulmonary oedema.
Zinc phosphide was mixed with the diet of rats at 0
(control), 50, 100, 200 and 500 mg/kg. Deaths occurred
at the two higher dosage regimens in 1/12 and 10/12
animals, respectively. There was a dose-dependent
reduction in haemoglobin, red cells and haematocrit
(WHO, 1988).
No long-term studies on phosphine and metal phosphide
exposure have yet been reported.7.2.3 Relevant in vitro data
No data available.7.2.4 Workplace standards
Occupational exposure limits for phosphine in
various countries are shown in Table 1. The
recommended exposure limits for phosphine in many
countries are higher than the registered regulatory
requirement. However, the exposure limits for
phosphine varies from 0. mg/m3 to 1.5 mg/m3 in
short-term exposure.Table 1 - Occupational exposure limits for phosphine in various
countries
Country Legal mg/m3 Comment
Australia Rec 0.4 TLV TWA
Belgium Rec 0.4 TLV
Bulgaria Rec 0.1 MPC
Czechoslovakia Rec 0.1 MAC TWA
0.2 MAC Ceiling value
Finland Reg 0.1 MPC TWA
Germany Rec 0.15 8.h TWA
0.3 5 min STEL
I.R.Iran Rec 0.3 TLV
Italy Rec 0.4 8.h TWA
Hungary 0.1
Netherlands Rec 0.4 TWA
1.5 STEL
Poland Reg 0.1 Ceiling value
Romania Reg 0.2 TWA
0.5 Ceiling value
Sweden Reg 0.4 1-day TWA
Switzerland Reg 0.15 TWA
United Kingdom Rec 0.4 8-h TWA
1.0 10 min TWA
USA Rec 0.4 TWA
1.0 STEL
USSR Reg 0.1 Ceiling value
Yugoslavia Reg 0.1 MAC TWA
Rec.=Recommendation
Reg.=Registered regulatory requirement
TLV=Threshold limit value
TWA=Time - weighted average
MPC=Maximum permitted concentration
MAC=Maximum allowable concentration
STEL=Short - term exposure limit7.2.5 Acceptable daily intake
Residues of phosphine or metal phosphides in
fumigated foods are considered negligible at 0.01
mg/kg or less. Reported various national and
international standards for phosphine residues in food
are 0.01 mg/kg (1 ppm) except for whole food grains in
India, for which the standard is 0.05 mg/kg. However,
the acceptable limit of phosphine residue in milled
food grain in this country was reported as 0.01 mg/kg.
Therefore the acceptable daily intake of
phosphine/phosphide residues could be extrapolated as
0.01 mg or less (WHO, 1988).7.3 CarcinogenicityNo data available.7.4 TeratogenicityNo data available.7.5 MutagenicityNo data available.7.6 InteractionsNo data available.8. TOXICOLOGICAL/TOXINOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS8.1 Material sampling plan8.1.1 Sampling and specimen collection
8.1.1.1 Toxicological analyses
Different sampling methods for
phosphine and the metal phosphides are
available.
I.Gaseous phosphine: Workplace air monitoring
and fumigation control demand a measurement
range from approximately 0.04 mg/m3 to
greater than the lower explosion limit of
25000 mg/m3. Thus, methods covering
concentrations differing by six orders of
magnitude are required. Techniques are
available that (a) directly indicate the
concentration in a grab sample or a
time-weighted average sample, (b) absorb or
adsorb phosphine from a known volume of air
for subsequent analysis directly or by
desorption and gas analysis and (c) give a
continuous record of time-dependent
concentrations. Some methods are given in
table 2.Table 2 - Methods of sampling and analysis
Method Range Efficiency Interference
ppm mg/m3Sampling
Silver nitrate 0.05-8.0 9.07-11.3 90%
(0.1 N)
impregnated paper
Ethanolic mercuric 0.05-3.0 0.07-4.2 NH3
chloride
Acidic potassium 0.01-0.05 100% H3S
permanganate (0.1N)
impinger
Silver diethyl- 0.6-18 0.85-25 54-86.2% H2S, AsH3,
dithiocarbomate SbH3
(0.5%) bubbler
Mercuric chloride 10-28 14-28 AsH3
(0.5%) aqueous
bubbler
Toluene impinger 41.5%
Mercuric chloride 0.05-2.5 0.07-3.5 88.0% SO2, H2S,
(0.1%) conductance AsH3, SbH3
cell
Silver nitrate 0.05-4.1 0.07-5.8 95% H2A, AsH3
impregnated
silica gel
Auric chloride 0.01-1000 0.014-1 400 100% AsH3, SbH3
impregnated
silica gel
Ethanolic mercuric 0.0006 88-100% AsH3, SO2,
chloride (0.1%) HCN, H2S
Mercuric cyanide 0.014-1.18 0.02-1.7 80%
impregnated
silica gel
Phosphine can be detected by filter paper
impregnated with a mixture of silver nitrate
and mercuric chloride. Direct-indicating
detector tubes are commercially available for
spot sampling.
There are directly-indicating continuous
samplers in which phosphine-containing gas is
passed through a paper tape impregnated with
a mixture containing silver nitrate which
develops a colour corresponding to the
phosphine concentrations.
II. Residues: Fumigated foodstuffs may
contain gaseous phosphine (adsorbed or in
trapped air) and residual aluminium or
magnesium phosphide. Interstitial and
adsorbed phosphine can be purged by nitrogen
and trapped in reagents for classical
analyses.
Total phosphine and phosphide is measured by
extraction of the fumigated stored product
with silver nitrate or with sulphuric acid.
The sulphuric acid method is preferred
because it also measures the capacity of the
product to release phosphine and this is of
more biological significance than the
measurement of free phosphine only.
III. Metal phosphide: Hydrolysis of metal
phosphides with acid yields phosphine, which
can be measured by any of the methods already
described.
IV. Inhaled expiration: Silver nitrate
impregnated paper test can be used for the
breath of patients exposed to phosphine.
Silver nitrate and phosphine react to form
silver phosphide which confirms the
diagnosis.
V. Gastric fluid: Gastric fluid (vomited or
through gastric tube) must be collected in a
clean glass tube or beaker for toxicological
analysis.
VI. Blood: Phosphine that is not excreted in
the expired air is oxidized and has no
significant effect on diagnosis. Thus blood
sampling for toxicological analysis may not
be required except for research purposes.
V. Urine: Oxidative metabolites mainly as
phosphite and hypophosphate may be present in
the urine . Urine sampling for the estimation
of the metabolites may be required.8.1.1.2 Biomedical analyses
Blood samples
In case of cardiac dysfunction, estimation of
cardiac enzymes including LDH and CPK may be
indicated. Biochemical analyses particularly
require liver and kidney function tests.
Urine samples including a 24-hour collection
are necessary to perform routine urine
analysis and to estimate creatinine clearance
and other investigations such as
beta-macroglobulin and N-acetyl beta-glucose
aminidase (NAG) as required.8.1.1.3 Arterial blood gas analysis
Arterial blood samples must be taken
for urgent estimation of PH, PaO2, PaCO2,
bicarbonate and the other parameters as usual
in severely poisoned patients in order to
assess and correct acidosis and pulmonary
dysfunction. Repeated sampling for arterial
blood gases may be required for the
management of patients with severe
phosphine/phosphide poisoning.8.1.1.4 Haematological analyses
Blood samples must be taken in the
usual haematology tubes for cell blood count,
haemoglobin, haematocrit. Estimation of
prothrombin time rate may be indicated
clinically.8.1.1.5 Other (unspecified) analyses
8.1.2 Storage of laboratory samples and specimens
8.1.2.1 Toxicological analyses
Blood and urine samples should be
stored at -20°C for further analyses.
However, no data are available on the
stability of phosphine/phosphides in
biological fluids.8.1.2.2 Biomedical analyses
8.1.2.3 Arterial blood gas analysis
8.1.2.4 Haematological analyses
8.1.2.5 Other (unspecified) analyses
8.1.3 Transport of laboratory samples and specimens
8.1.3.1 Toxicological analyses
Transportation of samples must
follow the required safety regulations.8.1.3.2 Biomedical analyses
8.1.3.3 Arterial blood gas analysis
8.1.3.4 Haematological analyses
8.1.3.5 Other (unspecified) analyses
8.2 Toxicological Analyses and Their Interpretation8.2.1 Tests on toxic ingredient(s) of material
8.2.1.1 Simple Qualitative Test(s)
Phosphine can be detected by filter
papers impregnated with a mixture of silver
nitrate and mercury (II) chloride. Aluminum
and magnesium phosphide can be hydrolysed
conventionally but zinc phosphide requires
acid hydrolysis to produce phosphine for
detection.8.2.1.2 Advanced Qualitative Confirmation Test(s)
Direct-indicating detector tubes are
commercially available for qualitative
confirmation of phosphine. Other
direct-indicating tubes of lower sensitivity
are available for the estimation of the
higher phosphine concentrations used in
fumigation.8.2.1.3 Simple Quantitative Method(s)
Colorimetric method is a simple
quantitative technique for phosphine. Filter
papers impregnated with a mixture of silver
nitrate and mercury (II) chloride which
detect phosphine can be made
semi-quantitatively by appropriate
configuration and measurement for stain
length of colour comparison. Calzodari
(1986) also reported a colorimetric method
involving oxidation of PH3 with bromine water
and reduction of phosphomolibate.
The quantity of phosphine bubbled through a
solution of mercury (II) chloride and
undergoing the reaction:
PH3.3HgCl2-----&gtP(HgCl)3 + 3 HCl
can be measured by the change in electrical
conductivity using a conductance cell or by
potentiometric titration of HCl against
NaOH.8.2.1.4 Advanced Quantitative Method(s)
Chan et al. (1983) reported a
headspace gas chromatographic technique using
a nitrogen phosphorus detector to estimate
phosphine applied to postmortem specimens
following ingestion of aluminum
phosphide.
Gas chromatography is the most sensitive
method for the determination of the phosphine
content of air samples.
Usually, samples are adsorbed from a solid
absorbent coated with mercury (II) cyanide,
although samples taken in syringes, gasbags
or tonometers can be used. Microcolorimetric
and thermionic detectors have detection
limits of 5000 and 20 pg, respectively. The
limit for flame photometric and argon and
helium beta-ionization detectors is 5 pg and
that for mass spectrometry is 1 ng.
Photoionisation detection is also commonly
used. Flame photometry combines both
sensitivity and stability.8.2.2 Tests for biological specimens
8.2.2.1 Simple Qualitative Test(s)
Silver nitrate impregnated paper
test can be used for the breath and gastric
fluid of the patients exposed to
phosphine/phosphides. Silver nitrate and
phosphide/phosphides react to form silver
phosphide which is dark grey (Chugh et al.,
1989). Blood and urine samples cannot be
used for phosphine detection, because
absorbed phosphine is rapidly oxidized and
excreted mainly as phosphite and
hypophosphite in the urine.8.2.2.2 Advanced Qualitative Confirmation Test(s)
8.2.2.3 Simple Quantitative Method(s)
8.2.2.4 Advanced Quantitative Method(s)
Khan et al. (1983) estimated
phosphine levels in post mortem specimens
liberated after acidification and found a
small amount in blood (0.5 ng/mL) and liver
(3 ng/g) but a large quantity (3000 ng/g) in
the stomach and contents. See also 8.2.1.4.
8.2.2.5 Other Dedicated Method(s)
8.2.3 Interpretation of toxicological analyses
Diagnosis of phosphine/phosphide poisoning is
normally based on the history of exposure and clinical
manifestation. However, qualitative toxicological
analyses confirm the diagnosis and the quantitative
tests may be used for the evaluation of the severity
and prognosis.8.3 Biomedical investigations and their interpretation8.3.1 Biochemical analysis
8.3.1.1 Blood, plasma or serum
Kidney and liver function tests and
cardiac enzymes, particularly blood urea,
electrolyte, creatinine, bilirubin, alkaline
phosphatase, transaminases, lactic
dehydrogenases and creatine phosphokinase,
should be estimated in all patients
hospitalized after phosphine/phosphide
poisoning. Further investigation, such as
plasma cortisol level (Chugh et al, 1989) and
plasma renin activity (Chugh et al, 1990)
should only be done as clinically
indicated.
In case of zinc phosphide poisoning, serum
zinc concentration may be elevated
(Stephenson, 1967) - in this case, by 590 to
605 g/100 mL (Normal 120 to 200 g/mL). Serum
magnesium and aluminium concentrations may
also increase in Mg3P2 and AlP poisoning,
respectively.8.3.1.2 Urine
Routine urinalysis and further
investigations such as estimation of
beta-microglobulin, N-acetyl-glucose
aminidase (NAG) and 24 hour urine creatinine
are required to evaluate renal function.8.3.1.3 Other fluids
8.3.2 Arterial blood gas analyses
Serial arterial blood gas analyses may be
required in order to assess respiratory and acid-base
abnormalities and to correct them.8.3.3 Haematological analyses
Routine haematological tests such as cell blood
count, haemoglobin, haematocrit are required for all
patients with phosphide/phosphine poisoning. Further
investigations such as prothrombin time ratio should
be done as clinically indicated.8.3.4 Interpretation of biomedical investigations
Biochemical and haematological tests are
required to assess the effects of phosphine/phosphide
poisoning.The results should be considered in
conjunction with the clinical picture and other
paramedical investigation such as electrocardiogram
and chest X-ray. Re-evaluation of the patient's
condition and repetition of biomedical and
haematological tests may be necessary.8.4 Other biomedical (diagnostic) investigations and their
interpretationElectrocardiographic changes in phosphine poisoning were
reported by Roman and Dubey (1985), who found cardiac
arrhythmias, usually heart block and myocardial ischaemia.
Wilson et al. (1980) also found similar ECG and
echocardiographic changes in child after phosphine poisoning;
they reported a transient elevation of the MB fraction of
serum creatinine phosphokinase and focal myocardial
infiltration with necrosis and widespread small vessel injury
at postmortem.
Misra et al. (1988), in a study of 8 cases of attempted
suicide by ingestion of aluminum phosphide tablets, found
circulatory failure in all cases and cardiac arrhythmias in
three patients. ECG changes included sinus arrhythmia with
ST segment depression in leads II and III; AVF and T- wave
inversion in V5-V6; and premature complexes which were
followed by ventricular tachycardia.8.5 Overall interpretation of all toxicological analyses and
toxicological investigationsCardiac monitoring with serial ECG recording, as well as
the other investigations are required for poisoning by
phosphine/phosphide.Sample collection
Blood samples (10mL) for biochemical investigations are
usually collected in dry glass tubes without any
preservative. Blood samples for haematology should be
collected in anticoagulant tubes as instructed by the
laboratory. A 24-hour urine collection may be needed for the
estimation of creatinine and phosphine metabolite
concentrations.Biochemistry
Routine urinalysis, blood urea, electrolytes, creatinine,
bilirubin, alkaline phosphates, transaminases (ALT, AST),
lactic dehydrogenase (LDH), creatinine phosphokinase (CPK)
should be measured in all patients with phosphine/phosphide
poisoning. If the results are abnormal (high LDH and CPK or
renal dysfunction), further biochemical investigations (e.g.
LDH and CPK, urine creatine, beta-microglobulin,
N-acetyl-glucose aminidase) should be determined.Haematology
Cell blood counts (CBC), haemoglobin (Hb) and haematocrit
(HCT) should be investigated in all patients with
phosphine/phosphide poisoning. If there are any
abnormalities or signs of gastrointestinal haemorrhage, or
hepatic failure, CBC, Hb and HCT must be repeated and further
tests including platelet counts, and prothrombin time ratio
should also be performed.Arterial blood gas analyses
Arterial pH and blood gases should be investigated in all
patients with respiratory dysfunction. Repeated arterial
blood gas analyses may be required in order to correct pH and
blood gas abnormalities.Toxicological analysis
Exhaled air can be tested for phosphine by an impregnated
silver nitrate paper. The paper test can also be used to
identify phosphine in the gastric contents. Blood samples
are of no practical use for the estimation of
phosphine/phosphide, since absorbed phosphine is rapidly
oxidised in the blood. However, Chan et al. (1983) reported
postmortem blood concentrations of phosphine of 5 ng/mL.
Urine can be tested for the oxidative metabolites of
phosphine (phosphite and hypophosphite).Other investigations
Since phosphine initially affects the respiratory and
cardiovascular system, respiratory function tests
(spirometry), chest X-ray and ECG are required.
Cardiorespiratory monitoring in an ICU with serial ECG
recording is necessary in severe cases. Further
investigation such as electroencephalography (EEG) and
electromyography (EMG) should be performed as clinically
indicated.8.6 References9. CLINICAL EFFECTS9.1 Acute Poisoning9.1.1 Ingestion
Deliberate ingestion of the metal phosphides
particularly AlP (Phostoxin) and Mg3P2 tablets or
pellets for suicidal purpose is common in the
countries in which these fumigants are sold without
restriction. Oral use of zinc phosphide paste (Zelio)
for suicidal attempts is also common in some
countries, including Islamic Republic of Iran, and the
author has seen and treated many of these patients
(see 9.3).
Acute poisoning by phosphine and the metal phosphides
is common in some countries, particularly in India and
Iran. Phosphine poisoning is either occupational or
accidental, but the acute metal phosphides poisonings
are mainly suicidal (Vale & Meredith, 1983).9.1.2 Inhalation
Phosphine inhalation is the commonest route of
intoxication and may occur accidentally or
occupationally. The metal phosphides, particularly
AlP and Mg3P2 may be easily hydrolysed in moisture
and produce phosphine. Following oral ingestion of
the metal phosphides, phosphine produced in the
stomach may also be inhaled (see 9.3).9.1.3 Skin Exposure
Skin exposure is not a common route of
intoxication by phosphine and the metal phosphide,
because skin absorption is not significant.9.1.4 Eye contact
It seems that phosphine does not affect the
eyes significantly. There are no data available on
the effects of phosphine/phosphides on the eyes either
in animals or man.9.1.5 Parenteral Exposure
No data available.9.1.6 Other
No data available.9.2 Chronic poisoning9.2.1 Ingestion
No data available.9.2.2 Inhalation
No long-term studies of chronic exposure to
phosphine and the metal phosphides have been reported.
Chronic poisoning is generally occupational, but no
reports with evidence of chronic poisoning by
phosphine and the metal phosphine have been published.
Chronic effects include anaemia, bronchitis,
gastrointestinal disorders, speech and motor
disturbances, toothache, swelling of the jaw,
mandibular necrosis, weakness, weight loss and
spontaneous fracture have been reported but these are
by no means general (WHO, 1988). Complications of
acute poisoning may occur but are distinct from the
effects of chronic poisoning.9.2.3 Skin contact
No data available.9.2.4 Eye contact
No data available.9.2.5 Parenteral Exposure
No data available.9.2.6 Other
No data available.9.3 Course, prognosis, cause of deathThe initial clinical manifestations of mild phosphide
inhalation may mimic upper respiratory tract infection
including cough, feelings of cold, sore throat, tachypnea,
respiratory irritation and tightness of breath. Other
symptoms may include nausea, vomiting, diarrhoea, headache,
fatigue and dizziness. In severe exposure, lung irritation
with persistent coughing, ataxia, paraesthesia, tremor,
diplopia, hypotension, weak pulse and jaundice may also
occur. Very severe cases may progress to acute pulmonary
oedema, cardiac dysrhythmia, convulsion, cyanosis,
hypothermia followed by hyperthermia and coma. Severe
metabolic acidosis, cardiovascular collapse, oliguria,
proteinuria and finally anuria may occur which may require
haemodialysis.
Most severely poisoned patients may die within a few hours
due to cardiovascular collapse, myocardial injury or
pulmonary oedema.
In a study of acute phosphine poisoning aboard a grain
freighter, the predominant symptoms in 29 crew members and
two children were headache, fatigue, nausea, vomiting, cough
and shortness of breath (Wilson et al., 1980). Abnormal
physical findings included jaundice, paraesthesia, ataxia,
intention tremor and diplopia. Focal myocardial infiltration
with necrosis, pulmonary oedema and widespread small vessel
injury were found at postmortem examination of a dead child.
The surviving child showed ECG and echocardiographic evidence
of myocardial injury and transient elevation of the MB
fraction of creatinine phosphokinase.
Deliberate ingestion of the metal phosphides especially AlP
(Phostoxin) causes nausea, vomiting, retrosternal and
abdominal pain, tightness in the chest and coughing,
headache, dizziness and sometimes diarrhoea. In severe
cases, gastrointestinal haemorrhage, tachycardia,
hypotension, shock, cardiac arrhythmias, cyanosis, pulmonary
oedema, metabolic acidosis, convulsions and coma may
occur.
Clinical features of renal failure and hepatic damage
including oliguria, proteinuria, anuria and jaundice may
develop later if the patient survives. In 8 cases of
attempted suicides by ingestion of aluminum phosphide
tablets, the clinical picture consisted of acute gastritis,
peripheral vascular failure, cardiac arrhythmia, jaundice and
renal failure (Misra et al, 1988). Six patients died and
postmortem examination in two of them revealed pulmonary
oedema, gastrointestinal mucosal congestion, and petechial
haemorrhages on the surface of the liver and brain.
In 15 cases of aluminum phosphide poisoning reported by
Khosla et al. (1988), all had severe symptoms such as shock,
cardiac arrhythmias, pulmonary oedema, and renal failure, of
which, only 7 patients survived.
In a prospective study of 16 cases of aluminum phosphide
poisoning by Chopra et al. (1986), profuse vomiting, pain in
the upper abdomen and shock were the most common presenting
features. Only 6 patients succumbed to their illness.
Analysis of various prognostic factors revealed that
ingestion of aluminum phosphide tablets taken from a freshly
opened bottle was associated with a greater risk of fatal
outcome.
The mortality of attempted suicide by acute
phosphine/phosphide poisoning is 37 to 80% (Singh et al.,
1985; Chopra et al.,1988; Khosla et al., 1988.) in suicidal
patients. However, in occupational or accidental exposure to
phosphine, the mortality is much lower and depends on the
severity of exposure, age and other predisposing factors of
the patients.
Death, which may be sudden, usually occurs within four days
but may be delayed for one to two weeks. Acute metal
phosphide poisoning, particularly deliberate aluminum
phosphide (Phostoxin) poisoning, may cause death within a few
hours (Singh et al., 1985; Chopra et al., 1986; Khosla et
al., 1988; Misra et al., 1988).
Severity of phosphine/phosphide poisoning:
Deliberate ingestion of the metal phosphides, particularly
aluminum phosphide (Phostoxin), is usually more severe than
occupational phosphine intoxication. However, the clinical
severity of phosphine/phosphide poisoning could be classified
as follows.
(a) Mild exposure may present as slight respiratory,
gastrointestinal and neuropsychiatric disorders such as
cough, shortness of breath, nausea, vomiting, headache,
fatigue and dizziness.
(b) Moderate exposure may cause cardiovascular, renal and
hepatic dysfunction, as well as more severe respiratory,
gastrointestinal and neuropsychiatric involvement, e.g.
tachycardia, hypotension, persistent coughing, paraesthesia,
tremor, diplopia, ataxia, intention tremor, retrosternal and
abdominal pain, shortness of breath, oliguria, jaundice and
diarrhoea.
(c) Severe exposure may progress to shock, gastrointestinal
haemorrhage, pulmonary oedema, cardiac arrhythmias, metabolic
acidosis, cyanosis, convulsions and coma. Renal failure and
liver damage may also occur.
Common causes of death following phosphine/phosphide
poisoning are pulmonary oedema, cardiac arrhythmias and
myocardial injury. A secondary cause of death may be renal
failure.
Stephenson (1967) classified patients seriously poisoned by
phosphine into 3 groups: (a) those who die within a few hours
with pulmonary oedema (b) the majority of fatal cases who die
after about 30 hours, and (c) those who survive the first 3
days who may not be in danger, despite extensive liver damage
and renal dysfunction.9.4 Systematic description of clinical effects9.4.1 Cardiovascular
Cardiovascular effects of aluminum phosphide
poisoning were studied by Khosla, Nand and Kumar
(1988). Twenty-five cases of aluminum phosphide
poisoning were observed by the authors over a period
of 2 years; 16 cases (64%) had evidence of cardiac
dysfunction. Despite adequate treatment, 40% of the
patients died. Shock and cardiac dysrhythmia were the
main effects. In another study by Singh & Rastogi
(1989), out of 32 cases of aluminum phosphide
poisoning, cardiac arrhythmia (28), dyspnoea (25),
palpitation (25), cyanosis (12), hypotension (12) and
shock (15) were the main clinical manifestations.
Hypermagnesaemia due to myocardial and liver damage
occurred in 13 patients.
Roman & Dubey (1985) and Khosla et al. (1988) have
reported circulatory failure, cardiac dysrhythmias,
myocarditis and cardiac failure; the dysrhythmias
included complete heart block, atrial fibrillation,
chaotic atrial and ventricular tachycardia.9.4.2 Respiratory
The respiratory tract is a major target for
phosphine poisoning. The initial symptoms include
cough, sore throat, tightness in the chest,
retrosternal pain, dyspnoea, followed by persistent
coughing, pulmonary oedema and respiratory distress
syndrome which may induce mortality. In a study of 59
cases of phosphine poisoning by Harger & Spolyar
(1958), 26 patients died mainly due to respiratory
disorders. The commonest finding at autopsy was
congestion of the lungs with marked oedema.
Wilson et al. (1980), in a study of 2 children and 29
crew members aboard a grain freighter with phosphine
poisoning, reported cough, shortness of breath and
pulmonary oedema. On postmortem examination they found
pulmonary oedema and pleural effusion. Misra et al.
(1988) on postmortem examination in two patients,
found pulmonary oedema and desquamation of the lining
epithelium of the bronchioles. In a study by Khosla
et al. (1988) on 15 cases of aluminum phosphide
poisoning, pulmonary oedema was the main cause of
mortality in 7 patients.
Chugh et al. (1989) reported 4 cases of adult
respiratory distress syndrome (ARDS) following
aluminum phosphide poisoning. All their patients had
shock on admission and developed ARDS within 6 hours.
Exhalation of phosphine was detected by positive
silver nitrate test. In a study by Khosla and Nand
(1988) on 15 cases of aluminum phosphide poisoning,
pulmonary oedema was one of the main findings which
contributed to the cause of death in 8 patients.
Chemical pneumonia may also be associated with
pulmonary toxic effects.9.4.3 Neurologic
9.4.3.1 Central nervous system (CNS)
The CNS is a major target in
phosphine poisoning. Neurologic symptoms
included headache, vertigo, tremors, and
unsteady gait, progressing to convulsion,
coma and death. Wilson et al. (1980)
described CNS symptoms of acute phosphine
poisoning in 2 children and 29 crew members
aboard a grain freighter as headache,
fatigue, drowsiness, dizziness and
paraesthesia weakness, followed by tremor on
physical examination, intention tremor in 9
patients ataxia in 2 patients, convulsion and
coma in a child who died. Disturbances of
smell and taste, dizziness and other clinical
manifestations of phosphine poisoning were
observed in the workers at a large shipyard
in Norway (WHO, 1988).
Miara et al. (1988) described CNS effects in
8 cases of acute phosphine poisoning as
drowsiness (3), stupor (2) and delirium (1).
On postmortem examination, the brain was
markedly congested with areas of exudation,
and small haemorrhages were observed.9.4.3.2 Peripheral nervous system
Some patients with
phosphine/phosphide poisoning develop
paraesthesia, fatigue and weakness (Wilson et
al., 1980; Misra et al., 1988). Peripheral
neuropathy (neuritis) may occur, but no
studies of the effects of phosphine/phosphide
on the peripheral nervous system have been
reported.9.4.3.3 Autonomic nervous system
There is no evidence of direct toxic
effects of phosphine/phosphide on the
autonomic nervous system, but indirect
effects through the adrenal gland and the
central nervous system may induce
tachycardia, hypotension, shock, and
gastrointestinal disorders.9.4.3.4 Skeletal and smooth muscle
Transient elevation of MB fraction
of creatinine phosphokinase in a surviving
child with phosphine poisoning reported by
Wilson et al. (1980) revealed cardiac and
skeletal muscle involvement. Gastrointestinal
and vascular disorders, such as abdominal
pain and vascular collapse, may be associated
with smooth muscle constriction.9.4.4 Gastrointestinal
Initial symptoms following ingestion of the
metal phosphides, particularly aluminum phosphide are
nausea, vomiting and abdominal pain (Chopra et al.,
1986). As Misra et al. (1988) reported, within 5
minutes of ingestion of aluminium phosphide tablets,
patients develop epigastric pain and vomiting; dryness
of the mouth, abdominal cramp and diarrhoea may also
occur. In severe cases, haematemesis and melaena may
develop but gastrointestinal haemorrhage has not been
recorded as a cause of death (in phosphine/phosphide
poisoning). At autopsy, gastrointestinal mucosal
congestion and haemorrhage have been found.9.4.5 Hepatic
The liver may be affected by phosphine/
phosphide poisoning, but the effects are delayed and
rarely cause death. Jaundice may occur 24 hours or
more after exposure. In 31 cases of phosphine
poisoning studied by Wilson et al. (1980), jaundice
occurred in 52% of the patients. Liver function tests
were abnormal in a further 10 patients. Abnormalities
included elevations of transaminases (mainly SGPT) and
lactic dehydrogenase (5 patients).
Misra et al. (1988) found one patient with jaundice
among 8 patients with phosphine poisoning they
studied. The patient died because of renal and
hepatic failure and ventricular tachycardia. On
autopsy, petechial haemorrhages were seen on the
surface of the liver and histopathological examination
showed vascular degeneration of hepatocytes.9.4.6 Urinary
9.4.6.1 Renal
Toxic effects of phosphine and the
metal phosphides on the kidneys are rare and
may be delayed. In 31 cases of phosphine
poisoning studied by Wilson et al. (1980),
renal symptoms were not prominent.
Urinalyses of 30 patients revealed
abnormalities in 8, usually as microscopic
haematuria and bile in urine. None of these
abnormalities persisted and all patients
improved within a week except one child who
died due to cardiovascular and pulmonary
toxic effects.
Misra et al. (1988) found one patient with
acute renal failure of 8 cases of phosphine
poisoning reported. This patient developed
anuria with blood urea of 80 mg/dL and serum
creatinine of 3.5 mg/dL on the second day of
admission. Because of persistent anuria and
uraemia, the patient underwent peritoneal
dialysis but died 72 hours after admission
because of hepato-renal failure and
ventricular tachycardia. On postmortem
examination, the kidneys were congested with
focal areas of exudation and small
haemorrhages.
Chopra et al. (1986) reported one patient
with significant proteinuria (4.8 g/day)
which gradually disappeared over 10 days, and
another patient who developed renal
failure.
Plasma renin activity (PRA) is increased in
shock due to aluminum phosphide poisoning
(Chugh et al., 1990). An initially high PRA
continued to rise, probably due to slow
release of toxic phosphine gas, which was
detected by a positive silver nitrate paper
test. The rise in PRA was directly
proportional to the dose of aluminum
phosphide consumed and there was a direct
relationship between mortality and an
increased PRA. The authors concluded that
angiotensin converting enzyme inhibitors may
have a role in combating shock in AlP
poisoning.9.4.6.2 Others
No data available.9.4.7 Endocrine and reproductive systems
There is little information on the effects of
phosphine/phosphide on the endocrine and reproductive
systems. Adrenocortical involvement in aluminum
phosphide poisoning was studied by Chugh et al. (1986)
in 50 cases. A significant rise in plasma cortisol
(&gt 1048 nmol/L) was observed in 20 patients.
Postmortem examination in 10 patients revealed mild to
moderate adrenal cortex changes including congestion,
oedema, and cellular infiltration. There was no
evidence that adrenal insufficiency or haemorrhage was
the cause of shock in these patients.9.4.8 Dermatologic
There have been no reports of dermal symptoms
in phosphine/phosphide poisoning.9.4.9 Eye, ear, nose, throat
Local effects
There has been no reports on the local effects of
phosphine/phosphide on the eyes and ears. The
irritant effects of phosphine on the nose and throat
are probably trivial in comparison with those on the
lung. Initial clinical manifestations of mild
phosphine inhalation may mimic upper respiratory tract
infection, but these are overshadowed by the other
effects of phosphine poisoning including pulmonary,
gastrointestinal and cardiovascular disorders.9.4.10 Haematologic
The haematologic system is not a major target
in phosphine/phosphide poisoning. However, marked
congestion of the spleen with focal areas of exudation
and small haemorrhages were found during the post
mortem examination of a patient who died due to
phosphine poisoning, though this was not the cause of
death (Misra et al., 1988). A reduction in red blood
cells, haemoglobin and haematocrit due to phosphide
poisoning has been reported in animal experiments
(WHO, 1988) but the only report in humans was of a
patient who developed purpura, with transient
reduction of red blood cells, platelets and
haemoglobin which was ascribed to phosphine/phosphide
poisoning.9.4.11 Immunologic
No data available.9.4.12 Metabolic
9.4.12.1 Acid-base disturbances
Metabolic acidosis is a common
problem in severe phosphine poisoning,
although it has not been reported in
detail.9.4.12.2 Fluid and electrolyte disturbances
Fluid and electrolyte disturbances
may occur in severe phosphine/phosphide
poisoning, particularly hypokalaemia
associated with metabolic acidosis, renal
dysfunction, and hypermagnesaemia.9.4.12.3 Others
No data available.9.4.13 Allergic reactions
There has been a single case report of purpura
ascribed to phosphine poisoning. The platelet count
was reduced to 60,000/mm3 and red blood cell to
3.1 × 106/mm3. On recovery, both the platelet and
red cell counts increased to 210,000/mm3 and
4.8 × 106 /mm3, respectively.9.4.14 Other clinical effects
No data available.9.4.15 Special risks: Pregnancy, breastfeeding, enzyme
deficiencies
No data available.9.5. OthersNo data available.9.6 Summary10. MANAGEMENT10.1 General principlesManagement depends on the route of exposure and proper
first aid treatment must be performed.
(a) First aid
In case of phosphine inhalation, the patient must be removed
from the exposure site and rested. Rescuers should follow
fully safety procedures. If a patient is unconscious, place
in the semi-prone recovery position or otherwise maintain the
airway and give oxygen if required. If breathing stops,
immediately ventilate the patient artificially (mouth-to-
mouth/nose or mechanically with oxygen if available). If the
heart stops, begin cardiopulmonary resuscitation (CPR). The
patient must then be referred to the nearest medical centre
for further treatment (Vale and Meredith, 1983).
In case of ingestion of a metal phosphide, do not give milk,
fats or saline emetics by mouth. If the patient is conscious,
induce vomiting. After vomiting, administer activated
charcoal (50 g in water by mouth) if available. Early
clearance of zinc phosphide from the gut was recommended by
Stephenson (1967) although he found Zn3P2 in gastric
contents at autopsy when gastric lavage had been
performed.
(b) Medical treatment
1. Gastric lavage, with tracheal intubation if appropriate,
using 2% sodium bicarbonate solution (to limit hydrolysis of
zinc phosphide). Stephenson (1967) used copper sulphate as
the precipitation solution for gastric lavage for Zn3P2.
Indian authors (Chopra et al, 1986; Khosla et al., 1988;
Misra et al, 1988) applied potassium permanganate for gastric
lavage.
2. Activated charcoal or medicinal liquid paraffin may limit
absorption of phosphine and zinc phosphide respectively and
may be administered by mouth or stomach tube (although it did
not work in the patient reported by Stephenson,1967).
Repeated doses of activated charcoal together with sorbitol
(to avoid constipation) may be useful and has been used by
the author but has not been yet reported for phosphine/
phosphide poisoning.
3. Monitor and support vital functions, particularly
cardiovascular, respiratory, hepatic and renal functions.
Treat shock conventionally (Chopra et al, 1986; Khosla et
al, 1988). Dopamine and hydrocortisone succinate have been
used to overcome the shock.
4. Perform arterial blood gas analysis and correct
respiratory dysfunction by clearing the airways, giving
oxygen and perform artificial (mechanical) respiration if
required. Metabolic acidosis must also be treated by giving
sodium bicarbonate according to the results of arterial pH
and blood gas analyses.
5. Hepatic and renal failure should be treated as required,
with consultation with an experienced hepatologist and
nephrologist.10.2 Life supportive procedures and symptomatic treatmentDehydration and shock was treated by infusion of
dextrose-saline, dopamine hydrochloride and hydrocortisone
hemisuccinate by Khosla et al (1988). Severe metabolic
acidosis must also be promptly treated by giving intravenous
sodium bicarbonate. Calcium gluconate has been used as a
membrane stabilizing agent. It was effective in controlling
excitement and convulsions in some patients. However, if
convulsions do not respond to calcium, an anticonvulsant drug
such as diazepam should be administered intravenously.
Severe cases of phosphine/phosphide poisoning must be treated
in an intensice care unit (ICU) in which vital facilities,
particularly cardiopulmonary monitoring and resuscitation,
would be available. Mechanical respiration may be required
in severely poisoned patients. Unfortunately there is no
specific treatment for phosphine/phosphide poisoning.
Therefore, life supportive procedures and symptomatic
treatment should be applied whenever clinically indicated.10.3 DecontaminationDepending on the route of entry different procedures
for decontamination must be performed. In case of
inhalation, the patient must be removed from the contaminated
area. With the patient at rest, clear the airway and give
oxygen and artificial respiration as required. In the case
of metal phosphide ingestion, vomiting should be induced
while preparation is made for gastric aspiration and lavage.
Syrup of ipecac can be used as an emetic. Alternatively,
copper sulphate 0.5 g as 1% aqueous solution can be given and
has the additional theoretical benefit of forming insoluble
copper phosphide (Stephenson 1967). Indian physicians
(Chopra et al., 1986; Khosla et al., 1988, Misra et al.,
1988) have used potassium permanganate solution (1:1000) as
an oxidative agent for gastric lavage, although experimental
and clinical evidence is lacking.
It is obviously important to clear the metal phosphide (AlP.
Zn3P2, Mg3P2) from the entire gastrointestinal tract.
A large dose (100 g) of mineral oil is recommended, but it is
not always effective. In such circumstances the dose should
be repeated and, if necessary, followed by a magnesium
sulphate purge, bearing in mind that this may lead to further
water and electrolyte losses. Activated charcoal with
sorbitol (Medicoal) may be effective and 5 to 10 g should be
given every 2 to 3 hour by mouth or through a nasogastric
tube. Milk, fats and saline emetics must not be given as
they may induce more toxicity with phosphine/phosphide.10.4 EliminationSince observed phosphine/phosphide is rapidly oxidised
in the blood it seems that elimination techniques such as
forced diuresis, alkinisation, haemoperfusion and dialysis
will be ineffective. Stephenson (1967) reported that forced
diuresis was not effective in one patient. However,
correction of dehydration and metabolic acidosis by
intravenous administration of isotonic solution and sodium
bicarbonate is required. Repeated doses of activated
charcoal with sorbitol by mouth or through a nasogastric tube
(gastrointestinal dialysis) may be effective. Haemodialysis
is required for the treatment of acute renal failure which
may complicate phosphine poisoning.10.5 Antidote10.5.1 Adults
No antidote is available for phosphine/
phosphide poisoning.10.5.2 Children
No antidote is available for phosphine/
phosphide poisoning.10.6 Management discussionSince the exact mechanism of toxicity of
phosphine/phosphide poisoning is not clear in human beings,
no specific treatment is available. A review of the European
cases by Stephenson (1967) suggests that early vomiting
improves the prognosis. Two young women swallowed similar
quantities of zinc phosphide in a suicide pact. One woman
was induced to vomit by mechanical means shortly after
poisoning; she had only transient symptoms and recovered
completely. Her friend would not vomit and despite gastric
lavage one hour after poisoning, she died within 24
hours.
Early recognition and treatment of phosphine/phosphide
poisoning is therefore of great importance. Treatment of
shock and metabolic acidosis together with the intensive care
therapy of the cardiopulmonary effects are essential.11. ILLUSTRATIVE CASES11.1 Case reports from literatureCases of acute phosphine poisoning reported in the
literature were reviewed by Harger & Spolyar (1958). Since
1900, a total of 59 cases with 26 deaths have been recorded.
In 6 of 11 reports, cargoes of ferrosilicon were cited as the
source of phosphine and in these cases the victims were
passengers or crew members on the ships or barges concerned.
Other cases involved the exposure of welders to calcium
carbide and/or raw acetylene and of submariners to sodium
phosphide.
Stephenson (1967) reported a fatal case of zinc phosphide
poisoning and reviewed the European literature. A 37-year
old woman drank a mixture of 180 g zinc phosphide and water
with suicidal intent. The zinc phosphide was 85% technical
grade powder used by a game-keeper to prepare rodent baits.
Vomiting began one hour after ingestion and was frequent and
violent. She was discovered in a state of shock after about
5 hours. Her skin was cold and blue; blood pressure was
unrecordable and heart sounds were inaudible. Occasional
ronchi were heard over the right lung. The breath smelt of
phosphine; one pint of pungent black fluid, smelling of
phosphine was aspirated from her stomach. After this, her
rectal temperature was 92°F (33°C). Arterial blood gas
analysis is revealed severe metabolic acidosis corrected by
1200 mEq sodium bicarbonate over 8 hours. White blood cells
were 15000/mm3 with 94% neutrophils. Serum zinc
concentration was 590 to 605 ng/100 mL (normal 120 to 200
ng/100 mL). The ECG showed sinus tachycardia and slight S-T
depression in the left ventricular leads. Severe abdominal
pain, hepatic factor and refractory tetany persisted for
several hours. Urine output diminished; fever and tachypnea
preceded a rapidly developing confusional state and
unexpected cardiac arrest occurred 41 hours after ingestion.
Postmortem examination revealed congestion in all organs.
The lungs were oedematous, the gastric mucosa were deeply
haemorrhagic and some centrilobular necrosis of the liver and
patchy necrosis of the convoluted tubules of the kidneys were
observed.
Wilson et al. (1980) reported 31 cases of acute phosphine
poisoning aboard a grain freighter. These included 2
children, one of whom died. The predominant symptoms were
headache, fatigue, nausea, vomiting, cough and shortness of
breath. The abnormal physical findings included jaundice,
paraesthesia, ataxia, intention tremor, and diplopia. Focal
myocardial infiltration with necrosis, pulmonary oedema and
widespread small vessel injury were found at postmortem
examination.
Singh et al (1985) reported 15 patients who had ingested 1.5
to 9 g (mean 4.7 g) of phostoxin pellets or tablets
(containing 58% aluminum phosphide); 13 cases were attempted
suicides. Repeated vomiting and hypotension occurred in all
patients, and 13 were in shock on admission. Other common
features included impaired sensorium, restlessness,
tachycardia, tachypnea, pulmonary crepitations, oliguria,
anuria and jaundice. Half of the patients had raised blood
urea, creatinine, bilirubin and transaminases.
Electrocardiographic abnormalities were observed in 6
patients. Metabolic acidosis with blood pH values of 6.97 to
7.31 and bicarbonate of 4.6 to 14.5 m mol/L were present in
all 6 patients tested. Eleven patients died and postmortem
examination revealed upper gastrointestinal congestion and in
2 cases haemorrhagic fluid was present in the stomach. Lungs
were congested and heavy and showed fibrinous pulmonary
oedema. Examination of the liver revealed mild fatty
infiltration and areas of centrizonal in two cases with
haemorrhages in another.
Chopra et al. (1980) described 16 patients suffering from
aluminum phosphide poisoning which accounted for half the
total number of cases of acute poisoning in their medical
centre. Profuse vomiting, upper abdominal pain and shock
were the commonest presenting features. Six patients who had
taken unexposed tablets of AlP died because of cardiovascular
collapse, pulmonary oedema and acute renal failure.
Khosla et al. (1988) presented 25 cases of aluminum phosphide
poisoning in which 16 (64%) cases had evidence of cardiac
dysfunction; the mortality was 40%. Peripheral circulatory
failure, cardiac dysrhythmias, myocarditis and cardiac
failure were the main cardiovascular findings.
Misra et al. (1988) reported 8 cases of phosphine poisoning
following ingestion of aluminum phosphide tablets for
suicidal attempt. The clinical picture consisted of
gastritis, altered sensorium and peripheral vascular failure
in all cases, cardiac arrhythmia (3), jaundice and renal
failure (1 each). Six patients died with a mean hospital
stay of 19 hours. Post mortem examinations revealed
pulmonary oedema, vascular degeneration of hepatocytes,
dilatation of hepatic central veins and areas of nuclear
fragmentation.12. ADDITIONAL INFORMATION12.1 Specific preventive measuresThe most important factor in the safe handling of
phosphine and metal phosphides and in their formulation, is
proper work practices. Management should identify these,
provide training for the operatives, and ensure that these
practices are carried out. Personal protective measures
recommended to reduce the likelihood of absorption of
phosphide preparations include the wearing of:
(a) Synthetic rubber gloves
(b) Rubber boots
(c) Lightweight impervious overalls, and
(d) Suitable eye protection
Adequate washing facilities should be available at all times
during handling. Eating, drinking and smoking should be
prohibited during handling. The means to measure the
concentration of phosphine in the air should be available and
used as required. When necessary, respiratory protective
equipment should be worn. In fumigation, each operator or
other person liable to be exposed to the gas must be provided
with an efficient means of respiratory protection. Persons
exposed to magnesium or aluminium phosphide (or any other
readily hydrolysed phosphide), which may give rise to an
airborne dust, should be protected by respiratory protective
equipment. This should be protective against gaseous
phosphine, since hydrolysis of dust in the filter of a dust
mask or respirator may give rise to high phosphine exposure
(WHO, 88).
No occupational accidents have been reported since 1957. It
seems that the established safety precautions are
satisfactory. Stephenson (1967) recommended the prohibition
of sale and distribution of zinc phosphide to all but
experts. This should also apply to aluminum and magnesium
phosphides.
Wilson et al. (1980) pointed out that ship crew members who
work with toxic substances must be adequately educated in
preventive measures. Multilingual signs should be placed
aboard ships as a reminder of toxic hazards. Most important,
ship owners and masters ought, whenever possible, to consider
substitution of less toxic fumigation for such highly
poisonous agents as phosphine.
Singh et al (1985), suggested that since the mortality of
aluminum phosphide poisoning is so high and there is no
specific antidote, a less toxic but equally effective agent
should be sought to replace this lethal substance.
Chopra et al (1988) indicated that the United Nations
Organisation and its agencies WHO and FAO and others in
consultation with state governments should quickly take
appropriate steps to prevent further loss of lives as a
result of self-poisoning with aluminum phosphide.
Misra et al (1988) pointed out that the high mortality and
lack of specific antidotes should caution the authorities
dealing with the distribution and use of this pesticide.12.2 OtherLeaks, spillages, and residues
Small leaks and residues of compressed gas can be discharged
slowly to the atmosphere in the open air. Larger quantities
should be burned using an appropriate burner.
Spillages and residues of metal phosphides in containers will
evolve phosphine for several days by reaction with
atmospheric moisture. Respiratory protective equipment will
be required by those dealing with them.
Residues at the site of spillage should be washed away using
a large quantity of water and the area kept secure and well
ventilated until the gas is no longer measurable.
Combustible packages can be incinerated at high temperature
(&gt1000°C) using proper facilities. Containers should not
cleaned for re-use, but should be disposed of by deep burial,
at an approved site, well away from habitation and where
there is no danger of contamination of water sources (WHO,
1988). Sowunmi (1985) measured the phosphine residues on
cowpeas fumigated with phostoxin tablets and showed them to
be well below the 0.1 ppm tolerance limits for grain at all
treatment levels.
Calzolari (1990) compared the residue formation of phostoxin
(AlP) with magnesium phosphide (Mg3P2) and reported that
the latter left a much lower residue concentration, with no
detectable PH3 after 120 hours.13. REFERENCESArena, J.M., & Drew, R.H. (1986) Poisoning Toxicology, Symptoms,
Treatment. 5th edition. Illinois, Springfield, pp. 361-393.
Beliles, R.P.(1981) in: Patty's Industrial Hygiene and Toxicology
(eds: Clayton, G.D. and Clayton, F.E.) New York, John Wiley &
Sons. pp. 1228-1229.
Calzodari S G (1986) Colorimetric determination of residues of
phostoxin. Tecnica Molitoria:37(8):609-622 (In Italian with
English abstract).
Calzodari S G (1990) Residue problem after disinfestation of
cereals. Tecnica Molitoria 41(4):272-275 (In Italian with English
abstract).
Casarett L J (1991) Inorganic Rodenticide.In: Casarett and Doull's
Toxicology: The Basis Science of Poisons. New York Macmillan Press
Ltd, pp 566-569.
Chan L T F (1983) Phosphine analysis in post-mortem specimens
following ingestion of aluminum phosphide. J. Analyt. Toxicol.
7(4):165-167.
Chopra J S, Karla O P, Malik V S, Sharma R, & Chandna A (1988)
Aluminum Phosphide poisoning: a prospective study of 16 cases in
one year. Postgrad. Md. J. 62, 1113-1115.
Chugh S N, Ram S, Chug K, & Malhotra K C (1989a) Spot diagnosis of
aluminum phosphide ingestion: an application of a simple test.
J Assoc Physicians India 37(3): 219-220.
Chugh S N, Ram S, Mehta L K, Arora B B, & Malhotra K C (1989b)
Adult respiratory distress syndrome following aluminum phosphide
poisoning. J Assoc Physicians India, 37(4): 271-272.
Chugh S N, Ram S, Sharma A, Arora B B, Saini A S, & Malhotra K C
(1989c) Adrenocortical involvement in aluminum phosphide
poisoning. Indian J Med Res 90: 289-294.
Chugh S N, Ram S, Singhal H R, & Malhotra K C (1989d) Significance
of heart rate response in shock due to aluminum phosphide
poisoning. J Assoc Physician India 37(11): 708-709.
Chugh S N, Singhal H R, Mehta L, Chugh K, Sankar V, & Malhotra KC
(1990) Plasma renin activity in shock due to aluminum phosphide
poisoning. J Assoc Physicians India 36(8): 398-399.
Deichmann W B, & Gerard H W (1964) Toxicology of drugs and
chemicals. New York and London, Academic Press, p. 472.
Ellenhorn M J, & Barceloux D G (1990), Medical Toxicology. New
York and London, Elsevier, pp 1053-1054.
Gossel R E, Hodge H C, Smith R P, & Gleason M N (1977) Clinical
Toxicology of commercial products, Baltimore, The Williams and
Wilkins Co. Section III pp 275-279.
Grant W M (1974) Toxicology of the eye. 2nd ed. Illinois,
Springfield p.826.
Haddad L M, & Winchester J F. (1983) Clinical management of
poisoning and drug overdosage. Philadelphia and London W.B.
Saunders Co. pp. 805-806.
Harger R N & Spolyar L W (1985) Toxicity of phosphine with a
possible fatality from this poison. Am Med Assoc Arch Ind Health
18: 497-504.
Khosla S N, N an N & Kumar P (1988a) Cardiovascular complications
of Aluminum phosphide poisoning. Angiology 39(4):355-359.
Khosla S N, Nand N & Kohsla P (1988b) Aluminum Phosphide
poisoning.J Trop Med Hyg 91(4):196-198.
Misra U K, Tripathi A K, Pandey R & Bhargwa B (1988) Acute
phosphine poisoning following ingestion of aluminium phosphide.
Human toxicol 7:343-345.
Polson C J, Green M A, & Lee M R (1983) Clinical toxicology. 3rd
ed. London Pitman Books Ltd. pp 241-2.
Roman R, & Dubey M (1983) The electrocardiographic changes in
quick phosphine poisoning. Indian Heart J 37(3):193-195.
Singh S, Dilawari J B, Vashist R, Malhotra H S, & Sharma B K
(1983) Aluminum Phosphide ingestion. Br Med J 290 (6475):
1110-1111.
Singh R B, Rastogi S S, & Singh D S (1989) Cardiovascular
manifestations of aluminum phosphide intoxication. J Assoc
Physicians India 37(9):590-592.
Sowunmi O (1985) Phosphine residues on cowpeas fumigated with
phostoxin tablets. Bull Acad Nat Med (Paris) 169(6): 897-904 (In
French with English abstract).
Stephenson J B P (1967) Zinc phosphide poisoning. Arch Environ
Health 15:83-88.
Thienes W C, & Haley T J (1972) Clinical toxicology. 5th ed.
Philadelphia, Febiger. p. 193.
Vale J A, & Meredith T J, (1983) in: Clinical management of
poisoning and drug overdosage (eds: Haddad and Winchester).
Philadelphia,W.B.Saunders. pp. 805-806.
Wilson R, Lovejoy F H, Jaeger R J, & Londrigan P L (1980) Acute
phosphine poisoning aboard a grain freighter. JAMA 244 (2):
148-150.
World Health Organization (1988) Phosphine and selected metal
phosphides, IPCS, Environmental Health Criteria 73, WHO,
Geneva.14. AUTHOR(S), REVIEWER(S), DATE(S)Author: Professor Mahdi Balali-Mood
Director, Poisons Centre
Imam Reza Hospital
91735 Mashha
P.O. Box 348
Islamic Republic of Iran
Tel: 98-51-93034
Tlx: 512015 IR
Fax: 98-51-92083
Date: November 1991
Peer review: Cardiff, UK (September, 1996)
Editor: Dr M. Ruse (October, 1997)